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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5795_Библиотеки_им_академика_М_И_Перельмана.pdf
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
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13.6.6.2 Splenic Lobulations andClefts
Important to avoid confusion with adrenal or renal mass, scars or traumatic lesions.
13.6.7 Malformations
13.6.7.1 Asplenia
Definition
No spleen, rare, associated with other systemic malformations and syndromes.
US Finding
No spleen/splenunculus seen.
Note Thorough assess entire abdomen for small/ectopic spleens.
13.6.7.2 Polysplenia Syndrome
Definition
No normal single spleen, but multiple smaller organs, may be positioned in normal
left upper quadrant or ectopic, often mobile and prone to torsion and infarction.
Rare variant: right-sided position—may be confusing. Shape can vary.
US ndings same as in normal spleen.
Note In inverted abdominal or systemic situs, liver is positioned on left side and
spleen in right upper quadrant, often associated with spleen anomalies and
variations.
Associated abdominal anomalies: disruption of inferior vena cava, azygos con-
tinuation, pancreas variations, bowel malrotation and renal agenesis/hypoplasia.
Additionally there may be thoracic and cardiac anomalies.
13.6.7.3 Wandering Spleen
Definition
Slightly atypical shape, not normally xed by gastrosplenic/splenorenal ligament,
commonly positioned ectopically. Increased risk of torsion and infarction.
US ndings same as in normal spleen.
13.6.8 Splenomegaly
Definition
Increased size—see normal values.
Caused by infection (acute or chronic, bacterial or viral, other rarer organisms),
congestive in portal hypertension and cardiac insufciency, haemolytic anaemia
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M. Riccabona
and inltration/depositions in systemic and metabolic disease (e.g. mucopolysaccharidosis, glycogenosis, leukaemia, lymphoma).
Secondary to (large) cysts and abscesses.
US Findings
Depending on underlying disease, parenchymal structure normal or disrupted. May
be patchy and inhomogeneous.
Echogenicity mostly normal, may be decreased or increased. Sometimes
inhomogeneous.
In signicantly enlarged spleens, extended view techniques are helpful to mea-
sure entire length; 3DUS reported to be most accurate for volume assessment
(Fig.13.28).
Note
In splenomegaly carefully assess for potentially underlying causes (e.g. liver/portal
vein pathology and lymphoma/leukaemia) or additional ndings (e.g. ascites and
gallstone).
13.6.9 Trauma
Definition
Spleen injury common in blunt abdominal trauma in children and may lead to acute
haemorrhage.
Children often compensate even severe haemorrhage for signicant time to even-
tually deteriorate suddenly, making a thorough US investigation particularly valuable. Grading is available and should also be attempted when diagnosed by US, as
grade correlates with risk of complications (Table13.7).
US Findings
Potentially increased size due to subcapsular haematoma, which in early posttraumatic phase sometimes cannot be discriminated from normal spleen tissue; only
Fig. 13.28 Extended eld of view in
splenomegaly. Signicantly enlarged spleen only
measurable using extended eld of view US
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
Table 13.7 Splenic injury grading system
Grade I
Subcapsular haematoma <10% of surface area
Capsular laceration <1cm depth
Grade II
Subcapsular haematoma 10–50% of surface area
Intraparenchymal haematoma <5cm in diameter
Laceration 1–3cm depth not involving trabecular vessels
Grade III
Subcapsular haematoma >50% of surface area or expanding
Intraparenchymal haematoma >5cm or expanding
Laceration >3cm depth or involving trabecular vessels
Ruptured subcapsular or parenchymal haematoma
Grade IV
Laceration involving segmental or hilar vessels with major devascularisation
(>25% of spleen)
Grade V
Shattered spleen
Hilar vascular injury with devascularised spleen
Adapted from American Association for Surgery of Trauma
311
perisplenic uid or later phases with sedimentation of erythrocytes and complex
uid-like appearance of haematoma enables visualisation (Fig.13.29).
• aCDS Infantile type haemangioma—usually of splenic injury and haematoma/
acute bleeding (Fig.13.29c, f).
• Initially haematoma iso- or hyperechoic to spleen parenchyma, later turning
hypoechoic (Fig.13.29d).
• Contusions without haemorrhage often only exhibit regionally more inhomogeneous structure without demarcation of haematoma.
• In laceration contour disrupted—complex shape, disruption of parenchyma, may
reach central vessels.
• Reduced diaphragmatic motion (reexive-reactive)—helpful indirect sign—
potentially follow-up exam after 6–24h.
Normalisation of tissue will take weeks to months; gradually lesion becomes
increasingly hypoechoic and demarcated/cyst-like (Fig.13.30); secondary posttraumatic cysts or brous scar tissue may remain.
Note
Peritoneal uid only initially located perisplenic will distribute in entire
abdominal cavity depending on position although originating from spleen—thus location of intra-abdominal uid does not necessarily correlate with origin/site of injury.
312
cd
M. Riccabona
a
b
ef
Fig. 13.29 Spleen trauma/haematoma. A series of images demonstrating various appearances of
acute splenic trauma: only slight subcapsular/perisplenic uid (a, b) with poorly depictable and
hazy parenchymal lesion, regional perfusion alteration without depictable parenchymal changes
but subcapsular haemorrhage (c) and obvious parenchymal damage (d); (e) Obvious spleen haematoma reaching from subcapsular to central. Note associated complicated pleural effusion. (f)
CEUS superiorly demonstrates the deep laceration of the spleen, poorly visible on grey scale (split
image: left side grey scale, right side contrast image)
CDS
• Useful to assess vitality or areas with lack of perfusion, e.g. by disruption or
infarction.
• In follow-up useful to detect posttraumatic aneurysms or AVF, which may rupture and cause secondary haemorrhage (Fig.13.31).
abc
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
Fig. 13.30 Old splenic hematoma. (a) Old splenic trauma: slight subcapsular uid with cyst-like
necrotic parenchymal areas after laceration. (b) Complicated cyst with debris, (c) Small, less complicated posttraumatic cystic remnant with potentially somewhat irregular margins in subcapsular area
313
Fig. 13.31 Splenic posttraumatic AVF. (a) Splenic posttraumatic AVF on CDS, with obvious
depiction of the red-coded feeding artery. (b) CDS depicts aliasing at the AVF and demonstrates
the draining vein encoded in blue
Role of US
Therapeutically splenic injury is increasingly managed conservatively or with techniques that enable salvage of some splenic tissue. Thus imaging diagnosis, and
follow-up of splenic injury is particularly important.
Initially US most essential for depiction of free abdominal uid (FAST)—indica-
tion for surgery usually based on clinical grounds and indication for additional
imaging usually based on trauma history and severity, complemented by US ndings.
Note In early phase US may miss even signicant splenic injury, unless aCDS or
ce-US is performed.
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M. Riccabona
13.6.10 Splenic Infarction
Definition
Rare condition in children, most commonly associated with sickle cell anaemia.
Other causes: acute portal vein thrombosis (venous infarction), inltration,
inammation and trauma.
US Findings
Acute enlargement of spleen, initially even with normal echotexture. Secondary
heterogeneous inhomogenously patchy parenchymal echoes due to haemorrhage
and haemorrhagic infarction (Fig.13.32a). Increasingly hypoechoic-cystic aspect
on delayed imaging (Fig.13.32b).
(a)CDS
• Large/main infarcted vessels depictable by CDS.
• Infarcted splenic tissue, particularly in early phase, often only detectable by
aCDS or ce-US (Fig.13.32c).
13.6.11 Space-Occupying Lesions oftheSpleen
13.6.11.1 Cysts
Definition
• Congenital—dysontogenetic, part of systemic cystic disease, posttraumatic and
postinammatory (pseudocysts).
• Posttraumatic/infectious cysts may remain stable or diminish and resorb.
Congenital/systemic splenic cysts may grow concordant to spleen growth or even
more. In syndromatous or systemic cystic disease additional cysts may appear.
US Findings
• Simple cyst: smooth margins, sharp border, thin membrane, no central structures,
anechoic uid, often solitary (Fig.13.33).
• Epidermoid cyst: may contain some echoes, sedimentation phenomena occur.
• Complex cysts: polylobulated with septae, some irregular margin or thick mem-
brane, potentially nodular components—large variety of underlying conditions
to be considered (history? Echinococcosis or other unusual infection?).
Use CDS to differentiate vascular pathology from cysts.
Note
Potentially US-guided puncture of cyst for aspiration/diagnosis and therapeutic
instillation of various agents—a coaxial access with sealing of the access tract
helpful to prevent bleeding.
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
315
abc
Fig. 13.32 Splenic infarction. (a) Subacute splenic infarction in sickle cell anaemia: regional
alteration of tissue echogenicity reaching into periphery/subcapsular; some normal spleen tissue
left in the centre near the hilus. (b) Old splenic infarction—creates images similar to posttraumatic
changes, with cyst-like necrotic area. (c) aCDS demonstrates non-perfused, infarcted areas even in
a very early stage, where grey scale ndings may be very subtle or even not yet depictable
Fig. 13.33 Splenic cyst. (a) Axial and (b) longitudinal view of spleen with dysontogenetic cyst in
an infant. Note physiologically prominent adrenal gland and typical appearance of neonatal kidney in (b)
13.6.11.2 Inflammation andAbscess
Definition
Inammation usually diffuses and only seen as spleen enlargement (spleen often
involved in any infection throughout body—does not mean it is infected itself).
Abscess and focal, infections = rare condition in childhood, most commonly
observed in immunocompromised (oncology, etc.) patients or posttraumatically.
Most common causes: staphylococcus, salmonella, fungus and hydatid disease.
US and CDS Finding
Similar to complicated cyst—spheric space-occupying lesion, some irregular and hazy
margin, variable (often hypoechoic) echotexture depending on duration and underlying
condition (Fig.13.34). Usually no proper capsule visible; sometimes perifocal hyperaemia seen on aCDS.Potentially halo-like surrounding hypoechogenicity (target sign).
May cause secondary infarction of dependent area.
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Fig. 13.34 Splenic abscess/inltration.
Multiple hypoechoic spheric/round
parenchymal lesions in slightly enlarged
spleen—in this case these were fungal abscesses
during chemotherapy; however, any other small
abscess or inltration (e.g. in lymphoma or
granulomatous disease) may exhibit similar
images and is sonographically indistinguishable
M. Riccabona
Note Multiple abscesses may be confusing, sometimes cannot be differentiated
from necrotic changes after infarction—if no systemic proof for infectious cause
found, US-guided puncture and drainage may be an option. But splenic punctures
have considerable risk of haemorrhage—take proper precautions such as occlusion
of access tract by glue etc (see chapter US guided intervention).
13.6.11.3 Tumours andSpace-Occupying Lesions
Definition
• Rare. Haemangioma, hamartoma and lymphangioma/lymphangiomatosis (e.g.
Gorham–Stout disease) occur.
• Malignant solid tumours other than inltration in lymphoma/leukaemia
extremely rare (e.g. angiosarcoma).
• Inammatory pseudotumour may exhibit calcications.
• Involvement in storage disease or systemic granulomatous disease as well as rare
(tropical) infection may be difcult to distinguish from tumourous condition.
US Finding
Very commonly hypo- or hyperechoic, nodular, space-occupying lesions, sometimes with hyperperfusion (Fig.13.35).
Note Multinodular irregularities also seen in splenic inltration by metastatic or
systemic disease (e.g. metabolic disease, leukaemia, lymphoma, Langerhans cell
histiocytosis and Gorham–Stout disease—then sometimes cyst-like or tubular).
Manifestation of other systemic granulomatous disease should be considered for
DDx (e.g. tuberculosis, cat scratch disease and sarcoidosis).
13.6.11.4 Role ofUS
Ideal method for diagnosis and follow-up:
• Particularly if CEUS available.
Restrictions: in early posttraumatic setting without CEUS, denition of
underlying entity.
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
Fig. 13.35 Spleen haemangioma. Two focal
round hyperechoic areas within spleen
parenchyma consistent with splenic
haemangiomas
317
Additional/Alternate Imaging
• Ce-MRI/PET, rarer ce-CT—complementary imaging—optimal for lesion
detection (contrast enhanced techniques), also restricted for lesion
characterisation/entity denition.
• Scintigraphy.
13.7 Pancreas
13.7.1 Requisites
Preparation
• Fasted patient helpful for easier acoustic access.
• Measures to avoid gaseous bowel and shadowing by stomach content.
Positioning
• Commonly accessed in patient lying supine.
• Positioning manoeuvres (if tolerated) may be helpful—decubitus and semi-upright.
Transducers
• Usually curved array for general assessment.
• Sometimes sector transducer if very small sonographic window.
• Linear array for detailed assessment, standard in neonates and infants.
• Frequencies vary with age/necessary penetration depth.
13.7.2 Indication
Various conditions that either involve or affect pancreas:
• Malformation
• Inammation
• Trauma
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M. Riccabona
• Obstruction
• Cysts, rarely tumours
13.7.3 Course ofInvestigation
Access via median upper abdomen:
• Use left liver lobe as window for head of pancreas and body.
• Access via left upper quadrant.
• Use spleen as window to tail (see Fig.13.36c).
• Potentially ll stomach with tea/water/formula (see Fig.13.36b).
• Asking patient to take a deep breath sometimes helpful.
Tip Graded compression and scanning while patient standing upright (allows
transverse colon to descend) improves access.
Try to localise pancreas in midline, use coeliac trunk and abdominal aorta as well
as origin of mesenteric artery as reference structures.
Pancreas assessed in axial and sagittal sections, position may be slightly oblique
(more cranial to left):
• If only small access window, angulated transducer from this window to see head,
body and tail.
• Use splenic vessels as landmark for assessing tail (see Fig.13.36c).
• Use high-resolution imaging for visualising pancreatic duct and details of parenchyma/contour.
Try to visualise common bile duct and surrounding anatomy (PV, uid, retroperi-
toneal area, neighbouring vessels, adjacent stomach, etc.).
Fig. 13.36 Normal pancreas. (a) Normal neonatal pancreas with homogeneous echogenicity, measurement of head (++
and large left liver lobe as US window. (b) Normal pancreas (P), axial view accessed via full stomach
(M) after feeding to improve visualisation. (c) Axial transsplenic view to prominent pancreatic tail
1
), tail (++3) and common bile duct (++2). Axial view using graded compression